eMedicine Specialties > Emergency Medicine > Dermatology

Warts, Genital

Author: A Antoine Kazzi, MD, Chair and Medical Director, Department of Emergency Medicine, American University of Beirut, Lebanon
Coauthor(s): Rasha A Hindiyeh, MD, MBA, Researcher, Department of Dermatology, University of California, Irvine, School of Medicine
Contributor Information and Disclosures

Updated: Aug 17, 2009

Introduction

Background

Genital warts are an epidermal manifestation attributed to the epidermotropic human papillomavirus (HPV). More than 75 types of double-stranded HPV papovaviruses have been isolated thus far. Many have been linked directly to an increased neoplastic risk in men and women.

Approximately 90% of all genital warts are related to HPV types 6 and 11 (HPV-6, HPV-11). These are the least likely to have neoplastic potential.

Thirteen HPV types (ie, 33, 35, 39, 40, 43, 45, 51-56, 58) have a moderate risk for neoplastic conversion; HPV-16 and HPV-18 are considered high risk. This picture is complicated by the proven coexistence of many types in the same patient (10-15%), lack of adequate information on the oncogenic potential of many other types, and ongoing identification of additional HPV-related clinical pathology. For example, bowenoid papulosis, seborrheic keratoses, and Buschke-Lowenstein tumors —previously parts of the differential diagnosis of genital warts—all have been linked to HPV infections.

• Bowenoid papulosis consists of rough papular eruptions and is considered a carcinoma in situ. Eruptions can be red, brown, or flesh colored and may regress or become invasive.
• Seborrheic keratoses previously were considered a benign skin manifestation. These consist of rough plaques and have an infectious and an oncogenic potential.
• Buschke-Lowenstein tumor (giant condyloma) is a fungating, locally invasive, low-grade cancer attributed to HPV.

Pathophysiology

Human papillomavirus (HPV) invades cells of the basal layer of the epidermis, penetrating skin and mucosal microabrasions in the genital area.

A latency period of months to years may ensue. Following that period, viral DNA, capsids, and particles are produced. Host cells become infected and develop the morphologic atypical koilocytosis of genital warts.

Most frequently affected are the penis, vulva, vagina, cervix, perineum, and perianal area. These mucosal lesions occasionally can be found in the oropharynx, larynx, and trachea. HPV-6 even has been reported in other uncommon areas (eg, extremities).

Multiple simultaneous lesions are common and may involve subclinical states as well as different anatomic sites. Subclinical infections have an infectious and oncogenic potential.

Consider the possibility of sexual abuse in pediatric cases; however, remember that infection by direct manual contact or, rarely, by indirect transmission from fomites may occur. Additionally, passage through an infected vaginal canal at birth may cause respiratory lesions in infants.

Frequency

United States

Annual incidence is 1%, and genital warts are considered the most common sexually transmitted disease (STD). A 4-fold or more increase in prevalence has been reported in the last 2 decades; prevalence reportedly exceeds 50%.

International

Reports vary on international prevalence, but available data from England, Panama, Italy, the Netherlands, and other developed and underdeveloped countries show HPV infections to be at least as common internationally as in the United States.

Mortality/Morbidity

Mortality is secondary to malignant transformation to a carcinoma. This oncogenic potential, which is rare with HPV-6 and HPV-11 (the most commonly isolated viruses), reportedly triples the risk of genitourinary cancer among infected males.

• Human papillomavirus (HPV) infection appears to be more common and worse in patients with various types of immunologic deficiencies. Recurrence rate, size, discomfort, and risk of oncologic progression are highest among these patients. Secondary infection is uncommon. Latent illness often becomes active during pregnancy.
• Vulvar warts may interfere with parturition. Trauma then may occur, producing crusting or erythema. Acute urethral obstruction may occur in women.
• Bleeding has been reported due to flat warts of the penile urethral meatus (usually associated with HPV-16) and in the large lesions that can occur during pregnancy. Lesions may lead to disfigurement.

Sex

Both sexes are susceptible to infection. Overt disease may be more common in men (reported in 75% of cases); however, infection may be more prevalent in women.

Age

Prevalence is greatest in persons aged 17-33 years, with a peak incidence in persons aged 20-24 years.

Clinical

History

• Painless bumps, pruritus, and discharge are the chief complaints encountered with genital warts.
• Generally, two thirds of individuals who have sexual contact with a partner who has genital warts develop lesions within 3 months.
• A history involving multiple lesions, rather than a single isolated wart, is more common.
• Involvement of more than 1 area is more common.
• History may indicate previous or other current STDs.
  • Oral, laryngeal, or tracheal mucosal lesions (uncommon) presumably transfer through oral-genital contact.
  • History of anal intercourse warrants a thorough search for perianal lesions.
• Urethral bleeding or urinary obstruction (uncommon) may be the presenting complaint when the wart involves the meatus.
• Vaginal bleeding during pregnancy may be due to condyloma eruptions. Coital bleeding also may occur.
• Latent illness may become active, particularly with pregnancy and immunosuppression.
• Lesions may regress spontaneously, remain static, or progress.

Physical

• Single or multiple papular eruptions may be seen.
  • Eruptions can be pearly, filiform, fungating, cauliflower, or plaquelike.

• Lesions can be quite smooth (particularly on the penile shaft), verrucous, or lobulated.
• Some appear harmless; others have a more disturbing appearance.
• Multiple sites often are involved simultaneously.

• Color may vary from that of the skin to erythema or hyperpigmentation.
• Check for irregularities in shape, form, or color that may suggest melanoma or malignancy.
• Seek perianal lesions, particularly in patients with a history or risk of immunosuppression or anal intercourse.
• Search for evidence of other STDs (eg, ulcerations, adenopathy, vesicles, discharge).
• Genital warts have a propensity for the penile glans and shaft in men and for the vulvovaginal and cervical areas in women.

• Urethral meatus and mucosal lesions can occur.
• Some lesions are subclinical, and some are hidden by hair or in the inner aspect of uncircumcised foreskin.
• Although earlier reports have suggested otherwise, the presence of external genital warts warrants a thorough search for cervical and urethral lesions.
  • Such internal lesions have been found in more than half of females with external lesions.
  • Infected males have a 20% chance or more (in one report) of having subclinical urethral lesions.
  • More than 50% of female patients with external lesions have negative Papanicolaou test (Pap smear) results but positive HPV infection results using in situ hybridization.
• Pruritus may be a complaint.
• Discharge may be evident.

Causes

• Genital warts are caused by several of the epidermotropic HPVs.
  • HPV-6 and HPV-11 most commonly are isolated; however, many of the more than 60 types of HPV may cause condyloma.
  • Male sex partners of women with cervical intraepithelial neoplasia often have infections of the same viral type.
• Smoking, oral contraceptives, multiple sex partners, and early coital age are risk factors for acquiring genital warts.

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